TGFB1 and heart disorder: The two Smads pairs create a complex that binds to Smad 4, which leads the complex into the nucleus to promote expression of the TGFβ1, extracellular matrix, matrix metalloproteases, and myofibroblast‐related genes.[39, 40, 43, 44, 45] Several strategies to inhibit TGFβ1 signaling have been tested, with limited success.[36, 37, 46, 47] Therefore, identifying new targets that can control TGFβ1 signaling may have important therapeutic potential in heart disease.